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首页> 外文期刊>Journal of Cellular Physiology >Lipid signaling affects primary fibroblast collective migration and anchorage in response to stiffness and microtopography
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Lipid signaling affects primary fibroblast collective migration and anchorage in response to stiffness and microtopography

机译：主纤维母细胞脂质信号影响集体迁移和安克雷奇刚度和微貌

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摘要

Cell migration is regulated by several mechanotransduction pathways, which consist of sensing and converting mechanical microenvironmental cues to internal biochemical cellular signals, such as protein phosphorylation and lipid signaling. While there has been significant progress in understanding protein changes in the context of mechanotransduction, lipid signaling is more difficult to investigate. In this study, physical cues of stiffness (10, 100, 400?kPa, and glass), and microrod or micropost topography were manipulated in order to reprogram primary fibroblasts and assess the effects of lipid signaling on the actin cytoskeleton. In an in vitro wound closure assay, primary cardiac fibroblast migration velocity was significantly higher on soft polymeric substrata. Modulation of PIP2 availability through neomycin treatment nearly doubled migration velocity on 10?kPa substrata, with significant increases on all stiffnesses. The distance between focal adhesions and the lamellar membrane (using wortmannin treatment to increase PIP2 via PI3K inhibition) was significantly shortest compared to untreated fibroblasts grown on the same surface. PIP2 localized to the leading edge of migrating fibroblasts more prominently in neomycin‐treated cells. The membrane‐bound protein, lamellipodin, did not vary under any condition. Additionally, fifteen micron‐high micropost topography, which blocks migration, concentrates PIP2 near to the post. Actin dynamics within stress fibers, measured by fluorescence recovery after photobleaching, was not significantly different with stiffness, microtopography, nor with drug treatment. PIP2‐modulating drugs delivered from microrod structures also affected migration velocity. Thus, manipulation of the microenvironment and lipid signaling regulatory drugs might be beneficial in improving therapeutics geared toward wound healing.
机译：细胞迁移是由几个转导通路,包括传感和转换机械微环境线索内部生化细胞信号,如蛋白质磷酸化和脂质信号。重大进展在理解蛋白质转导的背景的变化,脂质信号更难以调查。在这项研究中,刚度的物理信号(10,100年,400年?micropost地形是为了操纵重组主要成纤维细胞和评估在肌动蛋白脂质信号的影响细胞骨架。主要心脏成纤维细胞迁移速度明显高于软聚合物根基。通过新霉素PIP2调制的可用性治疗迁移速度几乎翻了一番10 ?所有的刚度。粘连和片状膜(使用增加通过PI3K PIP2渥曼青霉素治疗抑制)相比显著最短未经处理的纤维母细胞种植在相同表面。成纤维细胞迁移更加突出新霉素所致细胞治疗。蛋白质,lamellipodin,没有任何变化条件。micropost地形块迁移,集中PIP2附近。内动态应力纤维,来衡量荧光光漂白后恢复,与刚度没有明显不同,微貌,也不与药物治疗。从microrod PIP2量调节药物传递结构也影响迁移速度。因此,微环境和操作脂质信号管制药物有利于提高治疗的对伤口愈合。

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